Cervicogenic headache (CEH) is a headache localized in the neck or occipital region with projections to the frontal and temporal regions. CEH has been described as early as 1926, but Sjaastad and colleagues were the first to give it the current name1,2 and to formulated diagnostic criteria.3–5 While the question of CEH as a separate diagnostic entity remains controversial,6 we have found that one can reliably distinguish CEH from primary headaches such as migraine and tension-type headache.7
Since the pathogenesis of CEH appears to have an anatomical basis in the cervical region,8 several surgical procedures aimed at reducing the nociceptive input at the cervical level have been attempted. These include operative decompression of occipital nerves and cervical nerve roots,9–11 occipital neurectomy,7,12,13 and botulinum toxin injections14 among others.
Alternatively, cervical epidural injections to block peripheral nerves with local anesthetics and glucocorticosteroids have been attempted.15–18 The goal of this technique is to remove the aseptic inflammation caused by such factors as radicular neuritis or the cervical muscles and vasculature caused by cataplasia and herniation of high cervical disks, which may be involved in the pathogenesis of CEH.19 Since epidural injections of high cervical vertebra can be associated with important adverse events20 and the efficacy of a single dose is questionable, the purpose of this study was to place a catheter into high cervical epidural space to evaluate the effect of the continuous administration of low-dose glucocorticosteroid.
Between September 2004 and September 2006, thirtyseven patients diagnosed with CEH by the Department of Pain, Xuanwu Hospital, China were included in the study. All patients were diagnosed with CEH according to the diagnostic criteria of Sjaastad et al.3 The criteria also included: an initial visual analogue scale (VAS) score of > 60 mm during a pain period; evidence of degeneration of cervical vertebra and C2-C6 disk herniation, bulge, or degeneration, and positive response to blocking of C2 and C3 for at least one week's duration. Patients were excluded from the study if pathologic fracture, cancer, or other diseases of the cervical vertebra were identified, and if the CEH was thought to be caused by diseases of the nervous system or other factors.
Patients initially diagnosed with CEH were requested to keep a diary describing the mean number of days with mild or moderate pain, the mean number of times severe pain occurred, and the mean oral dosages of non-steroidal anti-inflammatory drugs (NSAIDs) used to control the pain. After three months, patients returned to the hospital to have the catheter placed for continuous epidural administration of analgesics. Under the guide of either C-arm radiography or computer tomography (CT), a catheter with a steel wire was placed at C6-C7, C7-T1, or T1-T2 intervertebral space. The catheter was advanced approximately 8–12 cm into the anterior epidural space. To confirm correct placement of the catheter, 3–5 ml of contrast medium was injected. Lidocaine (100–200 mg), dexamethasone (1–2 mg), and saline were mixed together to achieve a total volume of 250 ml. This was infused at a rate of 5 ml per hour for lasting for 3–4 weeks. In addition, triamcinolone acetonide 5 mg (dilated with 5–10 ml saline) was administered once weekly for 3–4 weeks, then the catheters were removed.Patients were subsequently requested to continue writing in their diaries for 12 months following the placement of the epidural catheter. The same outcome measures were recorded (i.e., days with mild to moderate pain, occurrence of severe pain, and daily NSAIDs dosages).
Pain was measured using the visual analogue scale (VAS). Mild or moderate pain was considered 0–70 mm and severe pains were between 71 mm and 100 mm. According to the effect on daily life and work caused by the CEH-associated pain, a combined score with the VAS scores was devised: Grade 0 was no pain; grade 1 was gentle pain, VAS 10–30 mm, and no effect on daily life or work; grade 2 was mezzo pain, VAS 31–70 mm, and both daily life and work were affected; grade 3 was VAS 71–100 mm, and when the pain occurred, patients could not participate in work of life.
The results were presented as mean±standard deviation (SD). The mean number of days with mild or moderate pain per month, the mean occurrence of severe pain per month, and the mean oral dosages of NSAIDs per day for each month were compared between the three month period prior to the placement of the epidural catheter and at 1–3, 4–6, 12 months post-operatively using an unpaired Student's t test. In all cases P <0.05 was considered statistically significant.
Thirty seven patients diagnosed with CEH were included in this study including 16 men and 21 women. The mean patient age was 53 years (range: 31 to 73 years). The mean duration of chronic CEH headache was 5.6 years (range: 1 to 28 years).
During the three month period immediately prior to placement of the epidural catheter days with mild or moderate pain were (22.0±4.3) per month,the occurrence of severe pain was (3.20±0.75) times per month, and daily dosages of NSAIDs was (1267±325) mg. During the first three months after catheter placed, days with mild or moderate pain, occurrence of severe pain, and daily dosages of NSAIDs were (6.5±2.6) days, (1.00±0.33) times and (100±33) mg respectively, the results of second three months after catheter placed were (9.8±3.7) days, (1.3±0.2) times and (433±75) mg respectivly, all significantly decreased compared to the three month period immediately preceding the placement of the epidural catheter and administration of the lidocaine/corticosteroid combination. By 12 months, days with mild or moderate pain, occurrence of severe pain, and daily dosages of NSAIDs were (16.3±3.3) days, (2.2±0.45) times and (950±125) mg respectively (Table).
This retrospective study shows that the continuous epidural administration of local anesthetic and corticosteroid can control chronic CEH at least for 6 months. Previous studies have reported that a single epidural injection of local anesthetic plus corticosteroid is useful for CEH19 and that continuous epidural local anesthetic plus corticosteroid has a greater efficacy than a single injection of these drugs for the treatment of chronic cervicobrachial pain.15
Pain of the head referred from the cervical region may originate from one or more pain-sensitive anatomic structures or soft tissues. The pain most often originates in the upper cervical regions (C1-C3). The intervertebral disks of C2-C3 and C3-C4, the capsule of the intervertebral joints, ligaments, nerves, and nerve roots are all thought to be potential causes of CEH.21 In this study, all patients had herniation, bulge, or degeneration of C2-C3 and\or C3-C4, C4-C5, C5-C6 disks on MRI.
It is possible that the cervical intervertebral disk hernia or nucleus pulposus leakage could excite high cervical nerve roots and pulpous CEH. Anzai22 reported that nucleus gelatinous could increase the electric discharge of neurons of the cornu dorsal medullae spinalis of rat, which could cause the mechanical allodynia of legs of rat. This finding suggests that nucleus gelatinous may be a key factor leading to algesthesia. Kawakami et al23 found that thermohyperpathia and machine hyperpathia caused by injection of the fibrous ring or nucleus gelatinous into the epidural space may be provoked by increase of phospholipase A2 and nitrogen monoxidum. Intravenous injection of methylprednisolone could mitigate nucleus gelatinous injury to the nerve. The efficacy of epidural steroids for the treatment of low back pain is generally accepted mainly because these drugs can inhibit aseptic inflammation and neurotransmission within C-fibers.24
All of the 37 patients included in this retrospective study received approximately 1 mg of dexamethasone per day and 5 mg of triamcinolone acetonide per week. In the first three months, the patients only rarely used NSAIDs and an obvious decrease in the number of days with mild or moderate pain and occurrence of severe pain were noted. Continuous injection of dexamethasone may inhibit aseptic inflammation. When the treatment finished, aseptic inflammation returned as well as the symptoms.
Narouze found that lateral atlantoaxial intra-articular corticosteroid injections provided short-term analgesia for patients with pain originating from the lateral atlantoaxial joint.25 In another case-series, 47 patients suffering from CEH were treated with repetitive occipital nerve blockade. Of these, 41 patients (87%) required more than one injection to achieve six months of pain relief.19
The patients in the present study were also administered lidocaine (100–200 mg in every pump) which exerts a wide range of anti-inflammatory actions through their effects on cells of the immune system and others (e.g., microorganisms, thrombocytes, erythrocytes). The potent anti-inflammatory properties of local anesthetics are superior in several aspects to traditional antiinflammatory agents of the NSAID and steroid group and are associated with fewer undesirable adverse events. This has prompted clinicians to local anesthetics in the treatment of various inflammation-related conditions. Local anesthetics have proven successful in the treatment of such diseases as arthritis and herpes simplex infections.26
Saal et al27 found that activity of phospholipase A2 of herniated nucleus gelatinosus in 5 patients was as much as 1000 times plasma levels. All herniated nucleus gelatinosus confirmed by operation and the phlegmastic material leaked from the cataplastic disk resulting in not only an aseptic inflammation but also an immunoreaction which could have caused the nociceptive pain. At the same time, the nervous system could have released neuropeptides such as substance P, neurokinin A, calcitonin gene-related peptide (CGRP), or nerve growth factor (among others) which contributed to a positive feedback loop aggravating the aseptic inflammation and leading to radicular neuritis and pain.28,29 Regional injection of local anesthetics could block or interfere local environment about pain and block the "infernal circle" of pain.30 In this study, noticeable improvements in all three outcome measures during the first six months after the epidural administration of lidocaine and corticosteroids were noted. It is possible that the drugs leaked from the intervertebral foramina and had a nerolysis affect on the nerve roots. By the end of the twelfth month, no statistical difference in outcome measures was noted compared to the pre-treatment period. It is possible that the aseptic inflammation returned or due to the extensive history of CEH pain—the mean duration of CEH in this study was 5.6 years. Perhaps if patients are treated earlier, the pain can be more effectively managed by this technique.However, the shortcomings of this study worth noting include the fact that this is a retrospective study and that no control group was included.
In conclusion, the results supported the hypothesis that continuous epidural administration of a local anesthetic plus corticosteroid for the treatment of chronic CEH was effective. While suppression of the hypothalamicpituitary axis, immunosuppression, and gastroduodenal ulceration are important adverse events associated with corticosteroid administration,31 the dosages used in this study were well within the ranges described in literature.15,32,33 In addition, none of the patients reported any symptoms associated with corticosteroid-related adverse events.
Clearly, the mechanisms involved in CEH are complex and despite the availability of various treatments, the optimal treatment strategy has yet to be determined. Our research group is continuing to work hard on the technique described herein to optimize this strategy.
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